Social mobility from a comparative perspective between Europe and Latin America

Production of INCASI Project H2020-MSCA-RISE-2015 GA 691004This chapter presents a review of the analysis of social mobility in the international sphere (Europe and Latin America), with a particular focus on the partner countries of the INCASI network. To date, few studies have linked nations whose economic and social aspects are so dissimilar. As is usual in the specialized literature, the relationship between social origin and class destination is addressed. This is done by noting the comparisons made across the geographical areas. We review the analyses that have been made of the evolution of social fluidity as well as the distance between social classes within each country and the comparisons made between them. We compare the main theories that have inspired the study of social mobility to date: modernization theory, which predicts an increase in relative mobility rates, and invariance theory, which postulates the constancy of social fluidity. Special attention is devoted to the role played by the family, the state and the market in late industrialized countries. We study the difficulties for social change, i.e. upward mobility from one class to another, as well as the likelihood of reproduction in comparative terms. To do so, we link these mechanisms with the AMOSIT model. The advances in methodology, techniques, theory and data processing are highlighted

IκBβ acts to inhibit and activate gene expression during the inflammatory response

The activation of pro-inflammatory gene programs by nuclear factor-κB (NF-κB) is primarily regulated through cytoplasmic sequestration of NF-κB by the inhibitor of κB (IκB) family of proteins1. IκBβ, a major isoform of IκB, can sequester NF-κB in the cytoplasm2, although its biological role remains unclear. Although cells lacking IκBβ have been reported3, 4, in vivo studies have been limited and suggested redundancy between IκBα and IκBβ5. Like IκBα, IκBβ is also inducibly degraded; however, upon stimulation by lipopolysaccharide (LPS), it is degraded slowly and re-synthesized as a hypophosphorylated form that can be detected in the nucleus6, 7, 8, 9, 10, 11. The crystal structure of IκBβ bound to p65 suggested this complex might bind DNA12. In vitro, hypophosphorylated IκBβ can bind DNA with p65 and c-Rel, and the DNA-bound NF-κB:IκBβ complexes are resistant to IκBα, suggesting hypophosphorylated, nuclear IκBβ may prolong the expression of certain genes9, 10, 11. Here we report that in vivo IκBβ serves both to inhibit and facilitate the inflammatory response. IκBβ degradation releases NF-κB dimers which upregulate pro-inflammatory target genes such as tumour necrosis factor-α (TNF-α). Surprisingly, absence of IκBβ results in a dramatic reduction of TNF-α in response to LPS even though activation of NF-κB is normal. The inhibition of TNF-α messenger RNA (mRNA) expression correlates with the absence of nuclear, hypophosphorylated-IκBβ bound to p65:c-Rel heterodimers at a specific κB site on the TNF-α promoter. Therefore IκBβ acts through p65:c-Rel dimers to maintain prolonged expression of TNF-α. As a result, IκBβ^(−/−) mice are resistant to LPS-induced septic shock and collagen-induced arthritis. Blocking IκBβ might be a promising new strategy for selectively inhibiting the chronic phase of TNF-α production during the inflammatory response

Essential versus accessory aspects of cell death: recommendations of the NCCD 2015

Cells exposed to extreme physicochemical or mechanical stimuli die in an uncontrollable manner, as a result of their immediate structural breakdown. Such an unavoidable variant of cellular demise is generally referred to as ‘accidental cell death’ (ACD). In most settings, however, cell death is initiated by a genetically encoded apparatus, correlating with the fact that its course can be altered by pharmacologic or genetic interventions. ‘Regulated cell death’ (RCD) can occur as part of physiologic programs or can be activated once adaptive responses to perturbations of the extracellular or intracellular microenvironment fail. The biochemical phenomena that accompany RCD may be harnessed to classify it into a few subtypes, which often (but not always) exhibit stereotyped morphologic features. Nonetheless, efficiently inhibiting the processes that are commonly thought to cause RCD, such as the activation of executioner caspases in the course of apoptosis, does not exert true cytoprotective effects in the mammalian system, but simply alters the kinetics of cellular demise as it shifts its morphologic and biochemical correlates. Conversely, bona fide cytoprotection can be achieved by inhibiting the transduction of lethal signals in the early phases of the process, when adaptive responses are still operational. Thus, the mechanisms that truly execute RCD may be less understood, less inhibitable and perhaps more homogeneous than previously thought. Here, the Nomenclature Committee on Cell Death formulates a set of recommendations to help scientists and researchers to discriminate between essential and accessory aspects of cell death

When Does Diversity Trump Ability (and Vice Versa) in Group Decision Making? A Simulation Study

It is often unclear which factor plays a more critical role in determining a group's performance: the diversity among members of the group or their individual abilities. In this study, we addressed this “diversity vs. ability” issue in a decision-making task. We conducted three simulation studies in which we manipulated agents' individual ability (or accuracy, in the context of our investigation) and group diversity by varying (1) the heuristics agents used to search task-relevant information (i.e., cues); (2) the size of their groups; (3) how much they had learned about a good cue search order; and (4) the magnitude of errors in the information they searched. In each study, we found that a manipulation reducing agents' individual accuracy simultaneously increased their group's diversity, leading to a conflict between the two. These conflicts enabled us to identify certain conditions under which diversity trumps individual accuracy, and vice versa. Specifically, we found that individual accuracy is more important in task environments in which cues differ greatly in the quality of their information, and diversity matters more when such differences are relatively small. Changing the size of a group and the amount of learning by an agent had a limited impact on this general effect of task environment. Furthermore, we found that a group achieves its highest accuracy when there is an intermediate amount of errors in the cue information, regardless of the environment and the heuristic used, an effect that we believe has not been previously reported and warrants further investigation

A Novel Tool for Online Community Moderator Evaluation

This study introduces a new instrument for leadership evaluation in online forums and other online communities which was developed using a grounded approach. Questions that emerged from the literature were then evaluated to create hypotheses that guided the development of an instrument for moderator evaluation. The Moderator Evaluation Contingency Scale (MECS) is modified from Fiedler’s contingency model to determine if a moderator is more task- or relationship-oriented in his or her approach to moderation and interactions with other members of a community. The MECS was developed and tested on Reddit in 2013–2014 using random sampling for Forum selection, moderator selection, and interactions with users. A content analysis using the MECS to evaluate posts was found to be a viable measure of a moderator’s ability to perform tasks like removing content as well as his or her ability to interact with users. Bots were analyzed using the MECS as well to determine bias. Next steps include making the instrument available for use by social media and niche community sites, administrators, and other moderators

Ebolavirus Is Internalized into Host Cells via Macropinocytosis in a Viral Glycoprotein-Dependent Manner

Ebolavirus (EBOV) is an enveloped, single-stranded, negative-sense RNA virus that causes severe hemorrhagic fever with mortality rates of up to 90% in humans and nonhuman primates. Previous studies suggest roles for clathrin- or caveolae-mediated endocytosis in EBOV entry; however, ebolavirus virions are long, filamentous particles that are larger than the plasma membrane invaginations that characterize clathrin- or caveolae-mediated endocytosis. The mechanism of EBOV entry remains, therefore, poorly understood. To better understand Ebolavirus entry, we carried out internalization studies with fluorescently labeled, biologically contained Ebolavirus and Ebolavirus-like particles (Ebola VLPs), both of which resemble authentic Ebolavirus in their morphology. We examined the mechanism of Ebolavirus internalization by real-time analysis of these fluorescently labeled Ebolavirus particles and found that their internalization was independent of clathrin- or caveolae-mediated endocytosis, but that they co-localized with sorting nexin (SNX) 5, a marker of macropinocytosis-specific endosomes (macropinosomes). Moreover, the internalization of Ebolavirus virions accelerated the uptake of a macropinocytosis-specific cargo, was associated with plasma membrane ruffling, and was dependent on cellular GTPases and kinases involved in macropinocytosis. A pseudotyped vesicular stomatitis virus possessing the Ebolavirus glycoprotein (GP) also co-localized with SNX5 and its internalization and infectivity were affected by macropinocytosis inhibitors. Taken together, our data suggest that Ebolavirus is internalized into cells by stimulating macropinocytosis in a GP-dependent manner. These findings provide new insights into the lifecycle of Ebolavirus and may aid in the development of therapeutics for Ebolavirus infection

A Novel Role for IκBζ in the Regulation of IFNγ Production

IκBζ is a novel member of the IκB family of NFκB regulators, which modulates NFκB activity in the nucleus, rather than controlling its nuclear translocation. IκBζ is specifically induced by IL-1β and several TLR ligands and positively regulates NFκB-mediated transcription of genes such as IL-6 and NGAL as an NFκB binding co-factor. We recently reported that the IL-1 family cytokines, IL-1β and IL-18, strongly synergize with TNFα for IFNγ production in KG-1 cells, whereas the same cytokines alone have minimal effects on IFNγ production. Given the striking similarities between the IL-1R and IL-18R signaling pathways we hypothesized that a common signaling event or gene product downstream of these receptors is responsible for the observed synergy. We investigated IκBζ protein expression in KG-1 cells upon stimulation with IL-1β, IL-18 and TNFα. Our results demonstrated that IL-18, as well as IL-1β, induced moderate IκBζ expression in KG-1 cells. However, TNFα synergized with IL-1β and IL-18, whereas by itself it had a minimal effect on IκBζ expression. NFκB inhibition resulted in decreased IL-1β/IL-18/TNFα-stimulated IFNγ release. Moreover, silencing of IκBζ expression led to a specific decrease in IFNγ production. Overall, our data suggests that IκBζ positively regulates NFκB-mediated IFNγ production in KG-1 cells